How Damaged Are N.F.L. Players’ Brains?

In November of 2010, a few dozen retired players from the National Football League gathered with their wives in a large living room. Snacking on appetizers and soft drinks, they listened to an informal pitch by John Hart, Jr., a neurologist at the University of Texas at Dallas. He wanted to scan their brains.

Since that first meeting, Hart’s team has recruited more than fifty former N.F.L. players for an ongoing study tracking their brain connections and mental health. The scientists’ latest batch of data, presented at a meeting of the Cognitive Neuroscience Society in San Francisco on April 15th, shows that retired N.F.L. players are more likely to have memory problems and depression than non-athletes of the same age, and that these deficits may stem from damage in certain bundles of white matter in the brain. But the researchers were more surprised by what the study didn’t show: nearly sixty per cent of the group had no mood issues, cognitive disability, or irregular brain patterns.

Hart’s is one of several studies released in the past few years looking at the neurological consequences of head trauma in collegiate and professional athletes. This research has already influenced athletic policies and treatment guidelines, and it may soon play a starring role in court.

In a Philadelphia courtroom on April 9th, a judge heard oral arguments for the N.F.L.’s motion to dismiss a lawsuit involving more than four thousand former players who claim that the league covered up the medical risks of repeated head injury. Over the next few months, U.S. District Court Judge Anita Brody is expected to decide whether the case should be dealt with in arbitration, as the league contends, or has standing in federal court. If she chooses the latter, litigation will drag on for years. And it’s almost certain that evidence from brain studies will be presented in the case—by both sides. “I think the lawyers could definitely use it either way,” said Ramon Diaz-Arrastia, an expert on brain injury from the Uniformed Services University of the Health Sciences, in Bethesda, Maryland.

When Hart’s study began, the sports world was reeling from some high-profile autopsy studies. Two research groups had found a striking pathology in the brains of more than a dozen former N.F.L. players, most of whom had died in middle age. Their brain tissue was littered with protein clumps that resemble those found in the brains of people with neurodegenerative disorders like Alzheimer’s. Buildup of this particular protein, called tau, is the signature feature of chronic traumatic encephalopathy (C.T.E.), a disease originally found in boxers and linked to a host of symptoms, from aggression and attention problems to muscle tremors and dementia.

The studies inspired a flurry of news reports and investigative reporting because of their obvious implications for the N.F.L., whose fans help generate more than nine billion dollars of revenue a year. But the work was controversial among some scientists because it relied on brain tissues from players who had committed suicide—such as the forty-four-year-old Andre Waters, who shot himself in the head—or from those with serious emotional issues, such as the forty-five-year-old John Grimsley, who accidentally shot himself in the chest while cleaning his gun.

The brain is full of nerve bundles, called white matter, which help transmit electrical messages between clumps of gray matter, the tissue that holds neurons. White-matter tracts are important for learning and memory retrieval. And they’re especially vulnerable to head injury; the brain floats in fluid and is tethered at the bottom by the brain stem and spinal cord, Hart explained. “Let’s say you’re running and you hit into something. Your skull stops but your brain keeps moving,” he said. “As it stretches forward and hits the front wall of the skull, it then sorta snaps back. When you do that, you stretch white matter.”

In a study published last month in JAMA Neurology, Hart’s team measured the strength of white-matter tracts and performed several cognitive and psychological tests in twenty-six former N.F.L. players. Another eight men took all of the behavioral tests, but were too claustrophobic to enter the coffin-like brain scanner. The average age of the group was sixty-two years old, and they had played in the N.F.L. for between two and fifteen years. All but two men had had at least one concussion (ranging from just a few seconds of confusion to several hours of lost consciousness), and the average was four concussions.

About forty-one per cent, or fourteen of the thirty-four former players, showed some kind of mild cognitive deficit. That’s vastly higher than the rate of about fifteen per cent in the general population; it is also not as bad as the researchers were expecting. “In the players with deficits, the deficits seem to be very, very mild, at worst,” notes study co-investigator Munro Cullum, a professor of clinical psychology at the University of Texas Southwestern. They had trouble remembering lists of words, for example, or copying a drawing they had seen twenty minutes earlier. Eight of the players, or twenty-four per cent, had depression, a rate about twice as high as the general population’s.

Among the players with cognitive deficits or depression, the researchers found weaker white-matter connections compared with controls of the same age. The findings are intriguing because they may be the root cause of the protein tangles seen in the postmortem studies, said Diaz-Arrastia, who wrote an editorial about the JAMA Neurology study for the journal. He points to similar studies of collegiate athletes finding disruptions in brain connectivity immediately following a concussion, like one published in 2011, in which researchers at Pennsylvania State University scanned the brains of seventeen rugby, ice hockey, and soccer players about ten days after they suffered concussions. The study found that several regions of their brains showed significantly weaker connections between the right and left sides.

What brain imaging hasn’t revealed so far is why head trauma affects some athletes and not others. “We need to investigate the effects of genetics,” said Maryse Lassonde, who worked as a neurological consultant for the Montreal Canadiens, a team in the National Hockey League, from 1999 until last year, and has scanned the brains of former college ice-hockey and football players. The N.H.L. was the first professional sports group to organize a systematic concussions-assessment program. Even a few years ago, Lassonde said, the players weren’t really aware of the risks of head injuries. Since then, a string of N.H.L. players committed suicide, and some were found to have C.T.E. And in 2011, Pittsburgh Penguins superstar Sidney Crosby was out of play for a year because of concussion injuries.

The science has changed policies at the N.F.L., too, after facing initial resistance from the organization. “In the old days, if a player wasn’t knocked unconscious, it was assumed they didn’t have an injury,” said Hunt Batjer, the chair of neurological surgery at the University of Texas Southwestern Medical Center and the co-chair of the N.F.L.’s Head, Neck, and Spine Committee. Often, they’d return to the game as soon as the dizziness wore off. Now they have days of medical evaluations and light exercise tests. “You can’t walk through the Cowboys locker room without seeing a flyer or poster about concussion now,” said Cullum, who is a consultant for the team.

Some insiders predict that the new scientific findings about the dangers of football will eventually kill the sport. In the face of negative media attention and impending lawsuits, the N.F.L. is throwing money into scientific research and ensuring it receives publicity for doing so. In 2010, it gave a million dollars to researchers at Boston University who were doing the autopsy work on C.T.E. in former players. (As of last year, these researchers had found evidence of C.T.E. in thirty-three out of the thirty-four brains tested.) Last year, the N.F.L. donated thirty million dollars to the National Institutes of Health. And in February, it announced a fifty-million-dollar partnership with General Electric to develop new imaging technologies for detecting concussions.

The focus of future research will be on identifying players who are most at risk, according to Batjer. For example, the league is piloting a study using tiny accelerometers, tucked away in the players’ mouthguards or helmets, to more precisely measure how forceful a collision has to be to cause neurological symptoms.

But the thousands of players (and players’ widows) suing the N.F.L. don’t think the league is doing enough to protect athletes from serious harm, or to help them with medical care after retirement. The plaintiffs also claim that the league deliberately concealed information about the neurological risks of concussion. Some retired players, though, don’t want anything to do with the lawsuits, arguing that a few years of glory on the field comes with an increased risk of health problems later on.

The split is evident between the two most eager participants in Hart’s study. Lee Roy Jordan, who was a linebacker for the Cowboys from 1963 to 1976, is reportedly part of the lawsuit against the N.F.L., while Daryl (Moose) Johnston, who played fullback for the team from 1989 to 1999 and is now a FOX sports analyst, has openly criticized the lawsuits.

If Hart has any opinions on the legitimacy of the suit, he’s keeping them to himself. He has served as an expert witness in the past. And if he’s asked to testify in this case? “I’ll let the data do the talking,” he says. “We’re Switzerland.”